Smooth Muscle Cells Flashcards

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1
Q

Characteristics of Smooth muscle cells

A

Spindle shaped, relatively small (about as long as a skeletal muscle is long)

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2
Q

Actin/myosin ratio in smooth muscle cells

A

Greater in smooth (10:1) vs skeletal (2:1)

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3
Q

What’s “missing” in smooth muscle cells?

A

Sarcomere, T-tubules, terminal cisternae, poorly developed SR. Lack hexagonal arrangement of actin/myosin

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4
Q

SR in smooth muscle

A

Still a Ca++ source, needs extracellular Ca++ source for contraction

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5
Q

Control of contraction in smooth muscle

A

Uses myosin-based control of contraction

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6
Q

Actin binding proteins of smooth muscle

A

Caldesmon and Calponin. not primary control proteins in smooth muscle

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7
Q

What is different about the troponin in smooth muscle?

A

No troponin -I to inhibit cross-bridge cycling

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8
Q

Polarity of myosin in smooth muscle?

A

Side-polar striated

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9
Q

Innervation of smooth muscle

A

Innervates by autonomic nervous system. No specialized nerve-muscle junction

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10
Q

Single unit smooth muscle organs

A

Unitary/visceral smooth muscle. Many gap junctions between cells. Behaves in syncytial manner. Sparse innervation.

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11
Q

Slow wave potentials

A

Spontaneous, graded oscillation in membrane potential that is rhythmical in nature, can lead to action potential

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12
Q

Plasticity

A

Slow stretch of single unit organs leads to lengthier of smooth muscle. Aka stress relaxation

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13
Q

Stretch induced contraction

A

Fast stretch cause depolarization and leads to contraction

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14
Q

Multi unit smooth muscles

A

Each cell acts relatively independent of other smooth muscle cells in the organ. More in specialized muscles (eye, bronchial muscle, GI sphincters). Less gap junctions. Tend to have higher innervation ratios.

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15
Q

High progesterone’ effect on smooth muscle

A

Reduces number of gap junctions in myometrial smooth muscle during pregnancy. Causes myometrium to behave more like non-innervated smooth muscle

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16
Q

Rising estrogen levels at term of pregnancy

A

Causes smooth muscle hypertrophy. Increase in number of gap junctions. Myometrial performs more like single unit

17
Q

What complex triggers contraction in smooth muscle?

A

Ca-calmodulin complex

18
Q

High amounts of cAMP does what to smooth muscle?

A

Relaxes smooth muscle (inactivated MLCK)

19
Q

High Ca and MLCK

A

Causes contraction by increasing MLCK activity

20
Q

Tone definition

A

Constant and stable low level of contraction

21
Q

Latch state

A

Maintains tone without ATP expenditure.

22
Q

What is ATP required for in smooth muscle contraction?

A

Control (light chain phosphorylation ) and cross bridge cycling

23
Q

Smooth muscle Ca extrusion

A

3Na/Ca exchanger, SR Ca ATPase

24
Q

Phospholamban

A

Inhibits Ca ATPase

25
Q

What happens if PLB is inhibited?

A

Increase in contraction due to lack of inhibition

26
Q

L-type of Ca channel

A

Opens slowly, open at relatively positive membrane potential. Affected by Ca channel blockers

27
Q

T-type Ca channels

A

open and close quickly. Rapid influx from channels may be key to Ca-induced Ca release from the SR. Not blocked by usual Ca channel blockers

28
Q

Difference in electromechanical coupling between smooth and skeletal muscle

A

Smooth has both local-graded potentials and action potentials

29
Q

cAMP-dependant relaxation

A

β-adrenergic agonist, adenosine, PGI2. Can occur with or without Ca. PKA phosphorylates MLCK thus preventing Ca-calmodulin complex. cAMP can also decrease Ca in some cells

30
Q

cGMP-dependant relaxation

A

NO, ANP. cGMP decreases myosin light chain phosphorylation. changes to phosphatase (increased) and MLCK (decreased) are mediated by phosphorylation of cGMP dependent protein kinase

31
Q

Phospholipase-C dependent contraction

A

Angiotensin II, α₁-adrenergic agonist, endothelium. IP3 is formed/releases intracellular Ca. DAG is made/activates PKC. Can phosphorylate and number of proteins to cause contraction.

32
Q

ATP-sensitive K-channels

A

K channel that remains closed in the presence of normal intracellular ATP

33
Q

Ischemia’s effect on intracellular processes

A

Decreases intracellular ATP, which opens the K-channels, and hyperpolarizes the membrane

34
Q

Hyperpolarization’s effect on voltage gated L-type Ca channels

A

Closed the channels, reducing Ca influx, and relaxes smooth muscle

35
Q

G-protein-coupled K channel agonists

A

ACh on the m2 receptors and adenosine on A1 receptors. Interacts with a G-protein

36
Q

G-protein subunit’s action on the K-channels

A

Bind directly to them and opens them. Cell is hyper polarized. L-type Ca channels are inactivated. Relaxation occurs